Kidney Response to the Spectrum of Diet-Induced Acid Stress

Nutrients. 2018 May 11;10(5):596. doi: 10.3390/nu10050596.

Abstract

Chronic ingestion of the acid (H⁺)-producing diets that are typical of developed societies appears to pose a long-term threat to kidney health. Mechanisms employed by kidneys to excrete this high dietary H⁺ load appear to cause long-term kidney injury when deployed over many years. In addition, cumulative urine H⁺ excretion is less than the cumulative increment in dietary H⁺, consistent with H⁺ retention. This H⁺ retention associated with the described high dietary H⁺ worsens as the glomerular filtration rate (GFR) declines which further exacerbates kidney injury. Modest H⁺ retention does not measurably change plasma acid⁻base parameters but, nevertheless, causes kidney injury and might contribute to progressive nephropathy. Current clinical methods do not detect H⁺ retention in its early stages but the condition manifests as metabolic acidosis as it worsens, with progressive decline of the glomerular filtration rate. We discuss this spectrum of H⁺ injury, which we characterize as “H⁺ stress”, and the emerging evidence that high dietary H⁺ constitutes a threat to long-term kidney health.

Keywords: alkali; base; bicarbonate; chronic kidney disease; diet; protein.

MeSH terms

  • Acid-Base Equilibrium
  • Acidosis / physiopathology*
  • Animals
  • Diet*
  • Dietary Proteins / administration & dosage
  • Disease Models, Animal
  • Glomerular Filtration Rate
  • Homeostasis
  • Humans
  • Hydrogen / urine
  • Kidney / physiology*
  • Kidney Diseases / physiopathology
  • Nephrectomy
  • Protons / adverse effects
  • Sodium Bicarbonate / administration & dosage
  • Stress, Physiological

Substances

  • Dietary Proteins
  • Protons
  • Hydrogen
  • Sodium Bicarbonate